The long-term objectives are to work out the neural wiring of the oculomotor system. Data are collected from human and animal experiments and interpreted in the form of control-systems models to try and provide mechanistic explanations for human oculomotor disorders. One specific aim is to try and locate the neural integrator that converts eye-velocity to eye-position commands. Lesions of the vestibular nucleus in monkeys may implicate this nucleus and recording from tonic cells in the reticular formation may reveal their involvement. The feasibility of the reverberating-collateral hypothesis for the integrator will be tested by a computer model. Another specific aim is to find whether or not plasticity of the vestibulo-ocular reflex (vor) is in the flocculus by surveying cell types in the cat flocculus, studying the appropriate types during visually-induced changes in the gain of the vor and the response of such cells to an interruption of climbing fiber signals from the inferior olive by injection of a local anesthetic. Another aim is to demonstrate plasticity in the human pursuit system by utilizing the dissociation of neural commands and eye movements that occur in muscle palsy and to incorporate the findings in a model of pursuit. Another aim is to record from burst neurons in the monkey that create vertical saccades and find out if their planes of action lie near those of the canals or eye muscles by rotating them in and around such planes to evoke quick phases. Another aim is to utilize very large eye and head movements to study and model the interaction of the vor and neural saccadic commands. The final aim is to demonstrate that subjects can cancel (suppress) their vor in roll. Since there is no torsional pursuit, this implies that there must exist a neurological system distinct from pursuit to cancel the vor. These projects are designed to quantify the behavior of human oculomotor subsystems, identify and describe new subsystems, describe interactions between them, and provide a neural scheme in the form of a model to explain their normal behavior. These measurements form a basis for the diagnosis of eye movement disorders in human beings and our hypotheses of signal processing by the neural substrates of these systems can often provide a hypothesis for the etiology of those disorders. These projects are also directed to studying the extent to which these systems can recover normal function following dysmetria caused by trauma or disease and the neural mechanisms underlying this plasticity.